Thrombotic complications after high dose intravenous immunoglobulin therapy in renal transplant patient

Department of Pathology, Yeungnam University College of Medicine, Daegu, Korea,
* Yong-Jin Kim
Department of Internal Medicine, Bong Seng Hospital, Busan
Joon-Seok Oh, Seung-Min Kim, Yong-Hun Sin, Joong-Kyung Kim

High-dose intravenous immunoglobulin (IVIg) commonly has been administered for the treatment of immunodeficiency or various inflammatory disorders, such as idiopathic thrombocytopenic purpura and autoimmune hemolytic anemia. It is recently recognized as a modifier of complement activation, which suggests IVIG would have clinical applications in solid organ transplantation for the desensitization and for the treatment of antibody-mediated rejection (AMR). Although high-dose IVIg generally considered safe, cases oflife-threatening thromboses in pulmonary, coronary, cerebral, and peripheral vessels have been reported.
A 46 year-old-women was hospitalized for 2nd renal transplantation from 59 year-old deceased donor. Prior to 2nd transplantation she received desensitization treatment with rituxan (200mg/body) and two times of high dose IVIG (1g/kg/day for 2days) because of 100% a panel reactive antibody (PRA) against class I HLA and 92% against class II antigens and several times of positive results of cross match test against T cells. Immediately after transplantation, allograft functioned well. On 14th postoperative day, creatinine was 1.6 and IVIG was administered to further reduce the allosensitization with the dose of 1g/kg/day for 2 days. No immediate acute toxic reactions during infusion were noted. Two days after IVIG, creatinine increased to 2.2. Biopsy was done and showed thromboembolisms in glomerular capillaries and segmental mesangiolysis in a few glomeruli (fi g 1,2). Four days after IVIG, the patient complained severe graft pain and the serum creatinine was 3.4, hemoglobin 9.4 and platelet count was 76,000. Emergency surgical exploration showed large perirenal hematoma with concomitant renal graft rupture. Transplant nephrectomy was performed. Microscopically, there was focal hemorrhagic infarction along with the rupture site and glomeruli showed segmental sclerosis with proliferation of podocytes and more advanced lesions of 1st biopsy fi ndings (fi g3).


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